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Biomedical subjects

M Cosentino

Publications and source records attributed to M Cosentino.

61 records · Page 4Linked to original sources
PubMedDate not supplied

Thyroid hormone and thyrotropin regulate intracellular free calcium concentrations in human polymorphonuclear leukocytes: in vivo and in vitro studies.

Intracellular free calcium concentrations (Ca++i) were studied in polymorphonuclear leukocytes (PMNs) from 13 athyreotic patients who had been previously treated by total thyroidectomy and radioiodine therapy for differentiated thyroid carcinoma, and from age- and sex-matched euthyroid healthy controls. Patients were studied twice, when hypothyroid (visit 1) and after restoration of euthyroidism by L-T4 TSH-suppressive therapy (visit 2). PMNs from patients at visit 1 had significantly lower resting (Ca++)i levels compared to both visit 2 and controls. Values at visit 2 did not differ from those of the controls. Stimulus-induced (Ca++)i rise was also significantly blunted at visit 1 and normalized at visit 2, possibly through a differential contribution of distinct intracellular Ca++ stores, as suggested by the response pattern to the chemotactic agent, N-formyl-Met-Leu-Phe (fMLP), to the selective SERCA pump inhibitor, thapsigargine, and to the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (FCCP). In vitro treatment of PMNs from healthy subjects with high TSH concentrations impaired intracellular Ca++ store function. Both resting (Ca++)i levels and fMLP-induced (Ca++)i rise increased in the presence either of low-concentration TSH or of T4, but effects of TSH and T4 were not additive. T3, rT3, and TRIAC had no effect. In conclusion, this study provides evidence for a direct relationship between thyroid status and (Ca++)i homeostasis in human PMNs, mainly related to direct actions of TSH and T4 on these cells.

Adult↗
PubMedDate not supplied

Prolonged monitoring of colonic spike activity by a computerized system: application to the rabbit colon.

In the present paper, we describe and validate a computerized system for the quantitative analysis of colonic spike activity in the conscious rabbit. This system allowed data acquisition at 160 Hz on 8 channels simultaneously during the recording session. Data analysis at the end of the recording session took approximately 10 min for each hour of recording. The spike recognition procedure was carried out on the basis of a discriminant function which discarded artifactual fast events. Data could be presented as histograms or be transferred into an ASCII file for later statistical analysis. Reliability tests showed that the misrecognition rate was only 3.88%. In conclusion, this computerized system is a reliable, timesaving tool for the quantitative analysis of colonic spike activity.

Action Potentials↗
PubMedDate not supplied

Measurement of catecholamines in mouse bone marrow by means of HPLC with electrochemical detection.

BACKGROUND AND OBJECTIVE: Noradrenergic innervation is present in the bone marrow and adrenergic agents can modulate hematopoiesis. However, since no data are available concerning endogenous catecholamines at this level, we investigated their presence and origin. METHODS: Using a high performance liquid chromatographic method, we have and measured endogenous catecholamines in bone marrow from normal, 6-OHDA-treated and pargyline-treated mice. RESULTS: Noradrenaline, adrenaline and dopamine levels were, respectively, 2806.74 +/- 408.85, 803.37 +/- 87.66 and 274.47 +/- 51.54 pg/g of tissue. Noradrenaline levels were lower after 6-OHDA (1130.47 +/- 142.73 pg/g of tissue, p < 0.01 vs. control values) and higher after pargyline (4122.62 +/- 509.54 pg/g of tissue, p < 0.05). None of these treatments significantly affected adrenaline or dopamine content. INTERPRETATION AND CONCLUSIONS: Noradrenaline in the bone marrow originates mainly from sympathetic nerve endings and is metabolized through specific enzymatic pathways. Adrenaline and dopamine may originate from other sources, such as the systemic circulation.

Adrenergic Agents↗